Neuroimmunological Colloquium @ AG Paul and NeuroCure/Charité Mitte

Dear Colleagues,

The next Neuroimmunological colloquium will take place on Monday, 30th January, 2017. This session will feature a talk by, Prof Dr. Michael Hoffmann from the University Eye Clinic, Otto von Guericke University, Magdeburg, Germany.

Topic: Electrophysiology of Visual Dysfunction


Venue: Campus Charité Mitte, Hufelandweg 6, Ferdinand Sauerbruch Hörsaal 4.

Time:  14:00


We provide continuing education credits by the Deutsche Ärztekammer and graduate student credits for Medical Neuroscience students.

Lunch and light drinks will be provided.

This year 2017 and for the rest of the Semester we have an exciting schedule of national and international presenters with expertise in diverse sub-areas of neuroimmunology.

Our hope is that this seminar will provide a platform to exchange ideas, create new collaborations, re-connect with colleagues and learn about the

novel research at the forefront of our neuroimmunology community.


Please feel free to forward the attached flyer to your colleagues and friends.


Looking forward to seeing you there!


Best regards,

Priscilla Koduah



Priscilla Koduah, PhD Candidate Neurodiagnostics Laboratory and Clinical Neuroimmunology Group NeuroCure Clinical Research Center Charité – Universitätsmedizin Berlin Charitéplatz 1 10117 Berlin, Germany Email:

Longitudinal Intravital Imaging of the Retina Reveals Long-term Dynamics of Immune Infiltration and Its Effects on the Glial Network in Experimental Autoimmune Uveoretinitis, without Evident Signs of Neuronal Dysfunction in the Ganglion Cell Layer

Bremer et al.

A hallmark of autoimmune retinal inflammation is the infiltration of the retina with cells of the innate and adaptive immune system, leading to detachment of the retinal layers and even to complete loss of the retinal photoreceptor layer. As the only optical system in the organism, the eye enables non-invasive longitudinal imaging studies of these local autoimmune processes and of their effects on the target tissue. Moreover, as a window to the central nervous system (CNS), the eye also reflects general neuroinflammatory processes taking place at various sites within the CNS. Histological studies in murine neuroinflammatory models, such as experimental autoimmune uveoretinitis (EAU) and experimental autoimmune encephalomyelitis, indicate that immune infiltration is initialized by effector CD4+ T cells, with the innate compartment (neutrophils, macrophages, and monocytes) contributing crucially to tissue degeneration that occurs at later phases of the disease. However, how the immune attack is orchestrated by various immune cell subsets in the retina and how the latter interact with the target tissue under in vivo conditions is still poorly understood. Our study addresses this gap with a novel approach for intravital two-photon microscopy, which enabled us to repeatedly track CD4+ T cells and LysM phagocytes during the entire course of EAU and to identify a specific radial infiltration pattern of these cells within the inflamed retina, starting from the optic nerve head. In contrast, highly motile CX3CR+1 cells display an opposite radial motility pattern, toward the optic nerve head. These inflammatory processes induce modifications of the microglial network toward an activated morphology, especially around the optic nerve head and main retinal blood vessels, but do not affect the neurons within the ganglion cell layer. Thanks to the new technology, non-invasive correlation of clinical scores of CNS-related pathologies with immune infiltrate behavior and subsequent tissue dysfunction is now possible. Hence, the new approach paves the way for deeper insights into the pathology of neuroinflammatory processes on a cellular basis, over the entire disease course.

Bremer et al. Front. Immunol., 23 December 2016

Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients

Pache & Zimmermann et al. from our lab just published a study investigating afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients. MOG-antibodies have recently been identified in a subgroup of patients with neuromyelitis optica and in patients with recurrent optic neuritis.

The paper has been published in Journal of Neuroinflammation 2016 13:282.

The study is part of a series of 4 papers describing different aspects of MOG-IgG in NMO and related disorders.

Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin
Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome
Part 3: Brainstem involvement – frequency, presentation and outcome
Part 4: Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients

Insufficient treatment of severe depression in neuromyelitis optica spectrum disorder

Neurol Neuroimmunol Neuroinflamm December 2016 vol. 3 no. 6 e286

In this just published study we investigated depressive symptoms and their current treatment in patients with neuromyelitis optica spectrum disorders in a collaboration with colleagues from Johns Hopkins University in Baltimore, MD, USA.


Objective: To investigate depression frequency, severity, current treatment, and interactions with somatic symptoms among patients with neuromyelitis optica spectrum disorder (NMOSD).

Methods: In this dual-center observational study, we included 71 patients diagnosed with NMOSD according to the International Panel for NMO Diagnosis 2015 criteria. The Beck Depression Inventory (BDI) was classified into severe, moderate, or minimal/no depressive state category. We used the Fatigue Severity Scale to evaluate fatigue. Scores from the Brief Pain Inventory and the PainDETECT Questionnaire were normalized to estimate neuropathic pain. Psychotropic, pain, and immunosuppressant medications were tabulated by established classes.

Results: Twenty-eight percent of patients with NMOSD (n = 20) had BDI scores indicative of moderate or severe depression; 48% of patients (n = 34) endorsed significant levels of neuropathic pain. Severity of depression was moderately associated with neuropathic pain (r = 0.341, p < 0.004) but this relationship was confounded by levels of fatigue. Furthermore, only 40% of patients with moderate or severe depressive symptoms received antidepressant medical treatment. Fifty percent of those treated reported persistent moderate to severe depressive symptoms under treatment.

Conclusions: Moderate and severe depression in patients with NMOSD is associated with neuropathic pain and fatigue and is insufficiently treated. These results are consistent across 2 research centers and continents. Future research needs to address how depression can be effectively managed and treated in NMOSD.

Afferent Visual Pathway Affection in Patients with PMP22 Deletion-Related Hereditary Neuropathy with Liability to Pressure Palsies.

PLoS ONE 0.1 371/journ al.pone.0164 617


Background: The PMP22 gene encodes a protein integral to peripheral myelin. Its deletion leads to hereditary neuropathy with liability to pressure palsies (HNPP). PMP22 is not expressed in the adult central nervous system, but previous studies suggest a role in CNS myelin development. The objective of this study was to identify potential structural and functional alterations in the afferent visual system in HNPP patients.

Methods: Twenty HNPP patients and 18 matched healthy controls (HC) were recruited in a cross-sectional study. Participants underwent neurological examination including visual acuity, visual evoked potential (VEP) examination, optical coherence tomography (OCT), and magnetic resonance imaging with calculation of brain atrophy, regarding grey and white matter, and voxel based morphometry (VBM), in addition answered the National Eye Institute’s 39-item Visual Functioning Questionnaire (NEI-VFQ). Thirteen patients and 6 HC were additionally examined with magnetic resonance spectroscopy (MRS).

Results: All patients had normal visual acuity, but reported reduced peripheral vision in comparison to HC in the NEI-VFQ (p = 0.036). VEP latency was prolonged in patients (P100 = 103.7±5.7 ms) in comparison to healthy subjects (P100 = 99.7±4.2 ms, p = 0.007). In OCT, peripapillary retinal nerve fiber layer thickness RNFL was decreased in the nasal sector (90.0±15.5 vs. 101.8±16.5, p = 0.013), and lower nasal sector RNFL correlated with prolonged VEP latency (Rho = -0.405, p = 0.012). MRS revealed reduced tNAA (731.4±45.4 vs. 814.9±62.1, p = 0.017) and tCr (373.8±22.2 vs. 418.7±31.1, p = 0.002) in the visual cortex in patients vs. HC. Whole brain volume, grey and white matter volume, VBM and metabolites in a MRS sensory cortex control voxel did not differ significantly between patients and HC.

Conclusion: PMP22 deletion leads to functional, metabolic and macro-structural alterations in the afferent visual system of HNPP patients. Our data suggest a functional relevance of these changes for peripheral vision, which warrants further investigation and confirmation.

New NIC schedule for Winter Term 2016/2017

Dear all,

our new schedule for our Neuroimmunology Colloquium (NIC) for this year’s winter term is final and available on this website.

We have put together an exciting mix from local, national and international speakers to give you a current update on topics in the context of our neuroimmunological research.

Hope to see you every Monday at 2 pm Charité Mitte Campus – Universitätsmedizin Berlin Ferdinand Sauerbruch Hörsaal 4, Hufelandweg 6.

The NIC will be part of the official teaching curriculum at Charité. Additional CME certification is pending.

NIC Winter 2016/2017 Schedule as PDF

October 17th Alexander Brandt, MD

NeuroCure Clinical Research Center, Charitè – Universitätsmedizin Berlin

Imaging Autoimmunity in the Central Nervous System

October 24th Charles Guttmann, MD

Center for Neurological Imaging, Harvard Medical School, Boston USA

International Platform for MRI Data Sharing

November 7th Tanja Schmitz-Hübsch, MD

Department of Neurology, Charitè – Universitätsmedizin Berlin

Motor Function of the Upper Limb: KINECT in Multiple Sclerosis

November 14th Martina Minnerop, MD

Institute for Neuroscience and Medicine, Jülich Germany

MR Morphometry in Cerebellar Ataxia

November 21th Doktorand Lunch Series

Julian Pohlan, Niesner Lab

Laura Pastura, Paul Lab

Bimala Malla, Infante-Duarte Lab

November 28th Klemens Ruprecht, MD

Department of Neurology, Charitè – Universitätsmedizin Berlin

Autoimmune Diseases of the CNS: Differential Diagnosis

December 5th Helena Radbruch, MD

Department of Neuropathology, Charitè – Universitätsmedizin Berlin

Role of B Cells and Antibody Producing Cells in Chronic Neuroinflammation

December 12th Michael Hoffmann, MD

University Eye Clinic, Otto von Guericke University, Madgeburg Germany

Electrophysiology of Visual Dysfunction

January 9th Velina Chavarro

NeuroCure Clinical Research Center, Charitè – Universitätsmedizin Berlin

Cognitive Function in Demyelinating Diseases

January 16th Doktorand Lunch Series

Silvina Romero, Infante-Duarte Lab

Frederike Oertel, Paul Lab

Karolin Pollok, Radbruch Lab

January 23rd Volker Siffrin, MD

Max-Delbrück-Centrum for Molecular Medicine, Berlin

Introduction to Basic Science – Neuroimmunology

January 30th Friedemann Paul, MD

Department of Neurology, Charitè – Universitätsmedizin Berlin

Pitfalls of Translational Research in Neuroimmunology – from Animal Models to Clinical Studies

New website

Dear visitor,

we are currently in the process of setting up a new web presents for the Neurodiagnostics Laboratory.

Until the new site is ready, you can access our old site or visit us on facebook.

Thank you!